Biomedical subjects

Zvi G Fridlender

Publications and source records attributed to Zvi G Fridlender.

6 recordsLinked to original sources

PubMed2005

Obstructing tracheal pulmonary Langerhans cell histiocytosis.

Pulmonary Langerhans cell histiocytosis, also known as eosinophilic granuloma, is an uncommon interstitial lung disease. A solitary nodule, usually parenchymal, may rarely be the only manifestation of the disease. We describe a case of Langerhans cell histiocytosis presenting as an obstructing tracheal lesion in a 55-year-old woman. Following complete resection of the lesion via flexible bronchoscopy, full recovery was achieved. This case represents a unique cause for tracheal obstruction, as well as an unreported manifestation of pulmonary Langerhans cell histiocytosis.

Female↗

PubMed2004

Recurrent infusion phlebitis induced by cyclosporine.

OBJECTIVE: To report a case of recurrent infusion phlebitis during cyclosporine treatment, which, as of October 14, 2004, is a previously unreported adverse effect of this drug. CASE SUMMARY: A 28-year-old man previously diagnosed with ulcerative colitis was admitted to the internal medicine department due to exacerbation of the condition and treated with intravenous hydrocortisone, followed by treatment with intravenous cyclosporine. During this treatment, the patient experienced quick, recurrent, and significant infusion phlebitis. The intravenous catheter and its site needed to be replaced repeatedly during the continuum of treatment, eventually leading to complete remission of the ulcerative colitis. After 8 months, the patient was still in remission, with no permanent signs of damage to the involved phlebitic veins. DISCUSSION: Infusion phlebitis induced by drugs is a common phenomenon that causes pain and difficulty in a patient's treatment. Many drugs, mainly antibiotics and cytotoxic drugs, have previously been reported to induce infusion phlebitis. We describe the first report of a patient with cyclosporine-induced recurrent infusion phlebitis. According to the Naranjo probability scale, the relationship of the encountered phlebitis to cyclosporine therapy is probable. CONCLUSIONS: Recurrent infusion phlebitis is a previously unreported adverse effect encountered during treatment with cyclosporine. This important adverse effect must be considered when treating patients with this unique drug.

Adult↗

PubMed2004

Myocardial infarction in a patient with beta-thalassemia major: first report.

Thalassemia is the most common hereditary anemia throughout the world. Survival in its most severe long-term form, beta-thalassemia major, has significantly risen in the last decades. Cardiac morbidity-heart failure and dysrhythmias-is still the most common cause of mortality in these patients. We describe herein a case of myocardial infarction with normal coronary arteries in a 48-year-old patient with beta-thalassemia and no other recognized risk factors for coronary artery disease. Thromboembolic phenomena, a known situation in these patients, occur at a frequency of 4-5%. However, as far as we know, this is the first report in the literature of myocardial infarction in association with beta-thalassemia. With the notable improvement in the life expectancy of thalassemia patients, ischemic heart disease may become an important complication encountered in these patients.

Electrocardiography↗

PubMed2003

Metastatic carcinoma presenting with concomitant eosinophilia and thromboembolism.

A case of a 58-year-old female patient who presented with significant blood eosinophilia and thromboembolic events is described. The patient was eventually diagnosed as suffering from a disseminated malignancy of gastrointestinal origin. Immunohistochemical studies of the tumor are presented. These studies show that tumor cells produce interleukin-3 and -5 and granulocyte macrophage-colony stimulating factor. These cytokines are known to support differentiation, proliferation, and survival of eosinophils. Their secretion is the probable explanation for the appearance of high blood eosinophilia in this patient. To the best of our knowledge, combined blood eosinophilia and thromboembolism as presenting manifestations of a solid tumor have never been reported.

Carcinoma↗

PubMed2002

Pleural effusion.

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Exudates and Transudates↗

PubMed2002

Resistance to adjuvant arthritis is due to protective antibodies against heat shock protein surface epitopes and the induction of IL-10 secretion.

Adjuvant arthritis (AA) is an experimental model of autoimmune arthritis that can be induced in susceptible strains of rats such as inbred Lewis upon immunization with CFA. AA cannot be induced in resistant strains like Brown-Norway or in Lewis rats after recovery from arthritis. We have previously shown that resistance to AA is due to the presence of natural as well as acquired anti-heat shock protein (HSP) Abs. In this work we have studied the fine specificity of the protective anti-HSP Abs by analysis of their interaction with a panel of overlapping peptides covering the whole HSP molecule. We found that arthritis-susceptible rats lack Abs to a small number of defined epitopes of the mycobacterial HSP65. These Abs are found naturally in resistant strains and are acquired by Lewis rats after recovery from the disease. Active vaccination of Lewis rats with the protective epitopes as well as passive vaccination with these Abs induced suppression of arthritis. Incubation of murine and human mononuclear cells with the protective Abs induced secretion of IL-10. Analysis of the primary and tertiary structure of the whole Mycobacterium tuberculosis HSP65 molecule indicated that the protective epitopes are B cell epitopes with nonconserved amino acid sequences found on the outer surface of the molecule. We conclude that HSP, the Ag that contains the pathogenic T cell epitopes in AA, also contains protective B cell epitopes exposed on its surface, and that natural and acquired resistance to AA is associated with the ability to respond to these epitopes.

Amino Acid Sequence↗